Linking systemic inflammation to periodontal disease: insights from blood-derived biomarkers in NHANES.

Periodontitis is a prevalent inflammatory disease linked to systemic immune activation and associated with various chronic conditions. Blood-derived inflammatory markers, such as the albumin-to-globulin ratio (AGR), may offer insights into systemic inflammation related to periodontitis, yet their role remains underexplored. This study aimed to investigate the association between AGR and other inflammatory markers with periodontitis in a representative U.S. adult population. A cross-sectional analysis was conducted using data from the National Health and Nutrition Examination Survey (NHANES) 2009 to 2014, including 10,135 adults aged ≥ 30 years with complete periodontal and laboratory data. Periodontitis was defined using CDC/AAP criteria. AGR, systemic immune-inflammatory index, neutrophil-to-lymphocyte ratio, lymphocyte-to-monocyte ratio and platelet-to-lymphocyte ratio were calculated from routine blood parameters. Associations between periodontitis and those inflammatory markers were assessed using multivariable logistic regression adjusted for sociodemographic, lifestyle, metabolic factors, systemic conditions, and liver function markers. Non-linear relationships were explored with restricted cubic splines. AGR was inversely associated with periodontitis in all models (Model 3: OR = 0.62, 95% CI: 0.49-0.78; P < 0.001). A significant L-shaped non-linear relationship was observed, with a threshold at AGR = 1.778. Below this value, each unit increase in AGR was associated with a 54% lower odds of periodontitis (OR = 0.46, 95% CI: 0.34-0.63). No significant non-linear associations were found for albumin, globulin, SII, PLR, or LMR. A significant gender interaction was detected (P < 0.001). Lower AGR was independently associated with greater odds of periodontitis, highlighting the potential role of systemic inflammatory biomarker in the pathophysiology of periodontitis. Longitudinal studies are needed to confirm causality.